Znaleziono wyników: 3

Liczba wyników na stronie

Wyniki wyszukiwania

Wyszukiwano:
w słowach kluczowych: apocynin

Sortuj według:

Ogranicz wyniki do:

Increased reactive oxygen species contributes to kidney injury in mineralocorticoid hypertensive rats

100%

Jin L., Beswick R. A., Yamamoto T., Palmer T., Taylor T. A., Pollock J. S., Pollock D. M., Brands M. W., Webb R. C.

Journal of Physiology and Pharmacology

2006

tom 57

nr 3

Hypertension is associated with increased reactive oxygen species (ROS). Renal ROS production and their effects on renal function have never been investigated in mineralocorticoid hypertensive rats. In this study we hypothesized that increased ROS production in kidneys from deoxycorticosterone (DOCA)-salt rats contributes to adverse renal morphological changes and impaired renal function in DOCA-salt hypertensive rats. We also determined whether ROS-induced renal injury was dependent on blood pressure. DOCA-salt hypertensive rats exhibited a marked increase in blood pressure, renal ROS production, glomerular and tubular lesions, and microalbuminuria compared to sham rats. Treatment of DOCA-salt hypertensive rats with apocynin for 28 days resulted in attenuation of systolic blood pressure and improvement of renal morphology. Renal superoxide level in DOCA-salt rats was 215% of sham-operated rats and it was significantly decreased to 140% with apocynin treatment. Urinary protein level was decreased from 27 ± 3 mg/day in DOCA-salt hypertensive rats to 9 ± 2 mg/day. 28 days of Vitamin E treatment also reduced renal injury in regard to urinary protein level and renal morphology but had no effect on blood pressure in DOCA-salt rats. Increased urinary 8-isoprostane, a marker for oxidative stress, in DOCA-salt hypertensive rats (55 ± 8 ng/day) was diminished by vitamin E treatment (24 ± 6 ng/day). These data suggest that renal injury characteristic of mineralocorticoid hypertension is associated with oxidative stress and is partly independent of blood pressure.

Rapid blood pressure increase after renal denervation in anaesthetized rats: interaction of oxidative stress and neuronal nitric oxide synthase

84%

Walkowska A., Vaneckova I., Sadowski J., Kompanowska-Jezierska E.

Journal of Physiology and Pharmacology

2019

tom 70

nr 4

A possible involvement of plasma membrane NAD[P]H oxidase in the switch mechanism of the cell death mode from apoptosis to necrosis in menadione-induced cell injury

67%

Niemczyk E., Majczak A., Hallmann A., Kedzior J., Wozniak M., Wakabayashi T.

Acta Biochimica Polonica

2004

tom 51

nr 4

The effects of inhibitors of plasma membrane NADPH oxidase on menadione-induced cell injury processes were studied using human osteosarcoma 143B cells. The intracellular level of superoxide in the cells treated with menadione for 6 h reached a maximum followed by an abrupt decrease. The population of apoptotic cells detected by Annexin V and propidium iodide double staining also reached its maximum at 6 h of menadione-treatment while that of necrotic cells increased continuously reaching 90% of the total population at 9 h of the treatment. Pretreatment of the cells with inhibitors of NADPH oxidase, including diphenyliodonium chloride, apocynin, N-vani- llylnonanamide and staurosporine was effective in lowering the menadione-induced elevations of superoxide, and also in the suppression of the switch of the cell death mode from apoptosis to necrosis in menadione-treated cells except for the case of staurosporine. These results strongly suggest that superoxide generated by NADPH oxidase, besides that generated by the mitochondria, may contribute to the remarkable increase in the intracellular level of superoxide in the cells treated with menadione for 6 h resulting in the switch from apoptosis to necrosis, although a direct evidence of the presence of active and inactive forms of NADPH oxidase in control and menadione-treated 143B cells is lacking at present.

Ograniczanie wyników

2 Journal of Physiology and Pharmacology

1 Acta Biochimica Polonica

1 Beswick R. A.

1 Brands M. W.

1 Hallmann A.

1 Jin L.

1 Kedzior J.

1 Kompanowska-Jezierska E.

1 Majczak A.

1 Niemczyk E.

1 Palmer T.

1 Pollock D. M.

1 Pollock J. S.

1 Sadowski J.

1 Taylor T. A.

1 Vaneckova I.

1 Wakabayashi T.

1 Walkowska A.

1 Webb R. C.

1 Wozniak M.

1 Yamamoto T.

1 2019

1 2006

1 2004

Wyniki wyszukiwania

Increased reactive oxygen species contributes to kidney injury in mineralocorticoid hypertensive rats

Rapid blood pressure increase after renal denervation in anaesthetized rats: interaction of oxidative stress and neuronal nitric oxide synthase

A possible involvement of plasma membrane NAD[P]H oxidase in the switch mechanism of the cell death mode from apoptosis to necrosis in menadione-induced cell injury